Cardiac Nestin + Mesenchymal Stromal Cells Enhance Healing of Ischemic Heart through Periostin-Mediated M2 Macrophage Polarization.

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  • Additional Information
    • Source:
      Publisher: Cell Press Country of Publication: United States NLM ID: 100890581 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1525-0024 (Electronic) Linking ISSN: 15250016 NLM ISO Abbreviation: Mol Ther Subsets: MEDLINE
    • Publication Information:
      Publication: 2017- : Cambridge, MA : Cell Press
      Original Publication: San Diego, CA : Academic Press, 2000-
    • Subject Terms:
      Cell Adhesion Molecules/*genetics ; Macrophage Activation/*genetics ; Macrophages/*metabolism ; Mesenchymal Stem Cells/*metabolism ; Myocardial Ischemia/*etiology ; Myocardial Ischemia/*metabolism ; Nestin/*metabolism ; Wound Healing/*genetics; Animals ; Biomarkers ; Cell Adhesion Molecules/metabolism ; Cell Differentiation ; Disease Models, Animal ; Genotype ; Immunophenotyping ; Mesenchymal Stem Cells/cytology ; Mice ; Mice, Transgenic ; Myocardial Ischemia/pathology
    • Abstract:
      Mesenchymal stromal cells (MSCs) show potential for treating cardiovascular diseases, but their therapeutic efficacy exhibits significant heterogeneity depending on the tissue of origin. This study sought to identify an optimal source of MSCs for cardiovascular disease therapy. We demonstrated that Nestin was a suitable marker for cardiac MSCs (Nes + cMSCs), which were identified by their self-renewal ability, tri-lineage differentiation potential, and expression of MSC markers. Furthermore, compared with bone marrow-derived MSCs (Nes + bmMSCs) or saline-treated myocardial infarction (MI) controls, intramyocardial injection of Nes + cMSCs significantly improved cardiac function and decreased infarct size after acute MI (AMI) through paracrine actions, rather than transdifferentiation into cardiac cells in infarcted heart. We further revealed that Nes + cMSC treatment notably reduced pan-macrophage infiltration while inducing macrophages toward an anti-inflammatory M2 phenotype in ischemic myocardium. Interestingly, Periostin, which was highly expressed in Nes + cMSCs, could promote the polarization of M2-subtype macrophages, and knockdown or neutralization of Periostin remarkably reduced the therapeutic effects of Nes + cMSCs by decreasing M2 macrophages at lesion sites. Thus, the present work systemically shows that Nes + cMSCs have greater efficacy than do Nes + bmMSCs for cardiac healing after AMI, and that this occurs at least partly through Periostin-mediated M2 macrophage polarization.
      (Copyright © 2020 The American Society of Gene and Cell Therapy. Published by Elsevier Inc. All rights reserved.)
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    • Contributed Indexing:
      Keywords: Periostin; immunomodulation; macrophage polarization; mesenchymal stromal cells; myocardial infarction
    • Accession Number:
      0 (Biomarkers)
      0 (Cell Adhesion Molecules)
      0 (Nestin)
      0 (Postn protein, mouse)
    • Publication Date:
      Date Created: 20200129 Date Completed: 20201225 Latest Revision: 20210305
    • Publication Date:
      20231215
    • Accession Number:
      PMC7054724
    • Accession Number:
      10.1016/j.ymthe.2020.01.011
    • Accession Number:
      31991111